The objectives of this project are to elucidate the biochemical mechanisms controlling the synthesis, storage, release, action and termination of action of neurotransmitters and to determine how genetic factors, environmental stimuli or drugs influence these control mechanisms. This year particular attention has focused on the interactions of prostaglandins with mechanisms which maintain cardiovascular function after hemorrhagic or endotoxin-induced shock. The release of renin appears to be enhanced by prostaglandins and seems essential for cardiovascular recovery when sympathetic mechanisms fail. Conversion of arachidonic acid to various physiological active compounds (prostraglandins, thromboxone, and leukotrienes) has been examined in SHR and WKY rats; the differences in effects of arachidonic acid appear to be a result of differences in reactivity of the animals to the metabolic products rather than due to differences in arachidonate metabolism.